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Aims: The role of revascularization in chronic coronary syndrome (CCS) and the value of ischaemia vs. anatomy to guide decision-making are in constant debate. We explored the potential of a combined assessment of ischaemic burden by vasodilator stress cardiovascular magnetic resonance (CMR) and presence of multivessel disease by angiography to predict the effect of revascularization on all-cause mortality in CCS., Methods and Results: The study group comprised 1066 CCS patients submitted to vasodilator stress CMR pre-cardiac catheterization (mean age 66 ± 11 years, 69% male). Stress CMR-derived ischaemic burden (extensive if >5 ischaemic segments) and presence of multivessel disease in angiography (two- or three-vessel or left main stem disease) were computed. The influence of revascularization on all-cause mortality was explored and adjusted hazard ratios (HRs) with the corresponding 95% confidence intervals were obtained. During a median 7.51-year follow-up, 557 (52%) CMR-related revascularizations and 308 (29%) deaths were documented. Revascularization exerted a neutral effect on all-cause mortality in the whole study group [HR 0.94 (0.74-1.19), P = 0.6], in patients without multivessel disease [n = 598, 56%, HR 1.12 (0.77-1.62), P = 0.6], and in those with multivessel disease without extensive ischaemic burden [n = 181, 17%, HR 1.66 (0.91-3.04), P = 0.1]. However, compared to non-revascularized patients, revascularization significantly reduced all-cause mortality in patients with simultaneous multivessel disease and extensive ischaemic burden (n = 287, 27%): 3.77 vs. 7.37 deaths per 100 person-years, HR 0.60 (0.40-0.90), P = 0.01., Conclusions: In patients with CCS submitted to catheterization, evidence of simultaneous extensive CMR-related ischaemic burden and multivessel disease identifies the subset in whom revascularization can reduce all-cause mortality., (Published on behalf of the European Society of Cardiology. All rights reserved. © The Author(s) 2021. For permissions, please email: journals.permissions@oup.com.)

Purpose: In ST-segment elevation myocardial infarction (STEMI) patients, longitudinal strain (LS) in remote non-infarcted myocardium (RNM) has not yet been characterized by tissue tracking (TT) cardiovascular magnetic resonance (CMR). In STEMI patients, we aimed to characterize RNM-LS by TT-CMR and to assess both its dynamics and its structural and prognostic implications., Methods: We recruited 271 patients with a first STEMI studied with TT-CMR 1 week after infarction. Of these patients, 145 underwent 1-week and 6-month TT-CMR and were used to characterize both the dynamics and the short-term and long-term structural implications of RNM-LS. Based on previously validated data, RNM areas were defined depending on the culprit coronary artery., Results: Reduced RNM-LS at 1 week (n = 70, 48%) was associated with larger infarct size and more depressed left ventricular ejection fraction (LVEF) at both the 1-week and 6-month TT-CMR (p value < 0.001). Late normalization of RNM-LS was frequent (28/70, 40%) and independently related to late recovery of LVEF (p value = 0.002). Patients with reduced RNM-LS at 1-week TT-CMR had more major adverse cardiac events (death, heart failure or re-infarction) in both the 271 patients included in the study group (26% vs. 11%, p value = 0.002) and in an external validation cohort made up of 177 STEMI patients (57% vs. 13%, p value < 0.001)., Conclusion: After STEMI, reduced RNM-LS by TT-CMR is common and is associated with more severe short- and long-term structural damage. There is a beneficial tendency towards recovery of RNM-LS that parallels late recovery of LVEF. More events occur in patients with reduced RNM-LS.

Infarct size (IS) at 1 week after ST-elevation myocardial infarction (MI) diminishes during the first months. The incremental prognostic value of IS regression and of scar size (SS) at 6 months is unknown. We compared cardiovascular magnetic resonance (CMR)-derived IS at 1 week and SS at 6 months after MI for predicting late major adverse cardiac events (MACE). 250 patients underwent CMR at 1 week and 6 months after MI. IS and SS were determined as the extent of transmural late enhancement (in >50 % of wall thickness, ETLE). During 163 weeks, 23 late MACE (cardiac death, MI or readmission for heart failure after the 6 months CMR) occurred. Patients with MACE had a larger IS at 1 week (6 [4-9] vs. 3 [1-5], p < .0001) and a larger SS at 6 months (5 [2-6] vs. 3 [1-5], p = .005) than those without MACE. Late MACE rates in IS >median were higher at 1 week (14 vs. 4 %, p = .007) and in SS >median at 6 months (12 vs. 5 %, p = .053). The C-statistic for predicting late MACE of CMR at 1 week and 6 months was comparable (.720 vs. .746, p = .1). Only ETLE at 1 week (HR 1.31 95 % CI [1.14-1.52], p < .0001, per segment) independently predicted late MACE. CMR-derived SS at 6 months does not offer prognostic value beyond IS at 1 week after MI. The strongest predictor of late MACE is ETLE at 1 week.

Background: Infarct size (IS) determined by cardiac magnetic resonance (CMR) has proven an additional value, on top of left ventricular ejection fraction (LVEF), in prediction of adverse arrhythmic cardiac events (AACEs) in chronic ischemic heart disease. Its value soon after an acute ST-segment-elevation myocardial infarction remains unknown. Our aim was to determine whether early CMR can improve AACE risk prediction after acute ST-segment-elevation myocardial infarction., Methods and Results: Patients admitted for a first noncomplicated ST-segment-elevation myocardial infarction were prospectively followed up. A total of 440 patients were included. All of them underwent CMR 1 week after admission. CMR-derived LVEF and IS (grams per meter squared) were quantified. AACEs included postdischarge sudden death, sustained ventricular tachycardia, and ventricular fibrillation either documented on ECG or recorded via an implantable cardioverter-defibrillator. Within a median follow-up of 2 years, 11 AACEs (2.5%) were detected: 5 sudden deaths (1.1%) and 6 spontaneous ventricular tachycardia/ventricular fibrillation. In the whole group, AACEs associated with more depressed LVEF (adjusted hazard ratio [95% confidence interval], 0.90 [0.83-0.97]; P<0.01) and larger IS (adjusted hazard ratio [95% confidence interval], 1.06 [1.01-1.12]; P=0.01). According to the corresponding area under the receiver operating characteristic curve, LVEF ≤36% and IS ≥23.5 g/m(2) best predicted AACEs. The vast majority of AACEs (10/11) occurred in patients with simultaneous depressed LVEF ≤36% and IS ≥23.5 g/m(2) (n=39)., Conclusions: In the era of reperfusion therapies, occurrence of AACEs in patients with an in-hospital noncomplicated first ST-segment-elevation myocardial infarction is low. In this setting, assessment of an early CMR-derived IS could be useful for further optimization of AACE risk prediction.

Background: T2 weighted cardiovascular magnetic resonance (CMR) can detect intramyocardial hemorrhage (IMH) after ST-elevation myocardial infarction (STEMI). The long-term prognostic value of IMH beyond a comprehensive CMR assessment with late enhancement (LE) imaging including microvascular obstruction (MVO) is unclear. The value of CMR-derived IMH for predicting major adverse cardiac events (MACE) and adverse cardiac remodeling after STEMI and its relationship with MVO was analyzed., Methods: CMR including LE and T2 sequences was performed in 304 patients 1 week after STEMI. Adverse remodeling was defined as dilated left ventricular end-systolic volume indexes (dLVESV) at 6 months CMR., Results: During a median follow-up of 140 weeks, 47 MACE (10 cardiac deaths, 16 myocardial infarctions, 21 heart failure episodes) occurred. Predictors of MACE were ejection fraction (HR .95 95% CI [.93-.97], p=.001, per %) and IMH (HR 1.17 95% CI [1.03-1.33], p=.01, per segment). The extent of MVO and IMH significantly correlated (r=.951, p<.0001). dLVESV was present in 40% of patients. CMR predictors of dLVESV were: LVESV (OR 1.11 95% CI [1.07-1.15], p<.0001, per ml/m(2)), infarct size (OR 1.05 95% CI [1.01-1.09], p=.02, per %) and IMH (OR 1.54 95% CI [1.15-2.07], p=.004, per segment). Addition of T2 information did not improve the LE and cine CMR-model for predicting MACE (.744 95% CI [.659-.829] vs. .734 95% CI [.650-.818], p=.6) or dLVESV (.914 95% CI [.875-.952] vs. .913 95% CI [.875-.952], p=.9)., Conclusions: IMH after STEMI predicts MACE and adverse remodeling. Nevertheless, with a strong interrelation with MVO, the addition of T2 imaging does not improve the predictive value of LE-CMR., (Copyright © 2012 Elsevier Ireland Ltd. All rights reserved.)

Background: Early stratification of patients according to the risk for developing microvascular obstruction (MVO) after ST-segment elevation myocardial infarction (STEMI) is desirable. We aimed to identify predictors of cardiovascular magnetic resonance (CMR)-derived MVO from clinical+ECG, laboratory and angiographic parameters available on admission., Methods: Characteristics available on admission were documented in 97 STEMI patients referred for primary angioplasty. MVO was determined using contrast-enhanced CMR., Results: MVO was present in 44 patients (45%). The C-statistic for predicting MVO was: clinical+ECG (.832), laboratory (.743), and angiographic parameters (.669). Adding laboratory to clinical+ECG information did not improve the C-statistic (.873 vs. .832, p=.2). Further addition of angiographic data (.904) improved the C-statistic of clinical+ECG (p=.04) but not of clinical+ECG and laboratory (p=.2). Independent predictors of MVO using clinical and ECG parameters were: Killip class >1 (OR 15.97 95%CI [1.37-186.76], p=.03), diabetes (OR 6.15 95%CI [1.49-25.39], p=.01), age <55years (OR 4.70 95%CI [1.56-14.17], p=.006), sum of ST-segment elevation >10mm (OR 4.5 95%CI [1.58-12.69], p=.005) and delayed presentation >3h (OR 3.80 95%CI [1.19-12.1], p=.02). A score was constructed assigning Killip class >1 2 points and the remaining indexes 1 point. The incidence of MVO increased with the score: 0 point: 8.7%; 1 point: 28.1%; 2 points: 71.4%; and 3+ points: 93% (p<.0001)., Conclusions: MVO can be predicted using parameters already available on patient admission. We developed a clinical-ECG score allowing for early and reliable classification of STEMI patients according to the risk of MVO., (Copyright © 2011 Elsevier Ireland Ltd. All rights reserved.)

To evaluate remote myocardial function after ST-elevation myocardial infarction (STEMI) and the impact of infarct size (IS) using cardiovascular magnetic resonance (CMR). 161 patients and 15 controls underwent CMR at 1st week and 6th month after STEMI. Using the 17-segments model, segments were categorized into infarcted, adjacent and remote myocardium. Relative systolic wall thickening (SWT, %) was assessed using the centerline method. IS (% of left ventricular mass) was determined in late enhancement imaging. Overall, in remote myocardium, SWT was comparable (83 ± 32) to controls (77 ± 25, P = .5) and did not increase significantly (P = .2) at the 6th month (88 ± 35, P = .3 vs. control). When IS was categorized into tertiles (<13.6%, (n = 49), 13.7-28.2%, (n = 60), >28.2%, (n = 52)), SWT in the remote area at the 1st week was not different from controls, regardless of infarct size (p between .2 and .8 for all tertiles). At 6 months, SWT was larger compared to controls only in small infarctions (98 ± 34 vs. 77 ± 25, P = .03). In medium and large infarctions there was no difference in SWT of the remote area compared to controls (87 ± 33 and 79 ± 34, P = .3 and P = .09) and there was no significant increase at 6 months (P between .2 and .9). In remote myocardium there was no difference in contractility compared to controls after STEMI. After 6 month a slight hypercontractility can only be observed in small infarctions. In medium and large infarctions no difference of SWT in remote myocardium compared to controls can be observed.